Nerve damage and degenerative nerve conditions affect those suffering from these conditions tremendously, depending on the severity of the symptoms. Traumatic injuries are a leading cause of nerve and spinal cord damage that can vary from minor self-healing to more severe symptoms such as constant pain up to complete loss of feeling or even paralysis. Functionally intact nerves maintain distinct ionic charges across their membrane, essentially existing as biobatteries that establish a distinct voltage separate from electrical conduction potential. When nerves are cut, the tissue no longer supports and separates charge, the potential to act as a battery is lost, and an injury current forms due to dissimilar material properties. The work of Galvani established the voltage-based understanding in the 18th century, and experiments since then have confirmed that injury currents exist and that the response at the cut ends of neurons diminishes the potential and inhibits repair because of voltage dissimilarity. Several explanations have been proffered to support regenerative strategies, among them a context of supporting tissue repair within an electrical field that sustains tissue gradients and prevents wound current and leakage. Similarly, neurological disorders involving neural cells are common among stroke victims wherein electrical signals evidencing brain activity in regions of the brain are lost.
Degenerative conditions in the brain and the nerves generally can cause similar loss of electrical activity in these tissues.
Efforts to reduce these symptoms or to repair, regenerate and reactivate cellular functioning of damaged or degenerative conditions is a priority in medicine. To date, application of autologous cells have met with only limited success. Similarly, allogeneic cells have not shown the promise of restoration nor gain of function from long term loss based on interrupted connection. The present invention discloses induction of nerve cells without participation of viable cells, and establishes a precedent for poly-ampholyte function that exhibits an electrolytic charge to preserve and protect the function of the allograft spinal cord tissue until it can be implanted. Previous patents have demonstrated the use of hydroxyl-ethyl starches (HES) as an appropriate carrier and delivery combination that helps retain the material in place during the repair process. Hydroxyethyl starch is an amylopectin-based modified polymer that has been used as colloidal plasma volume expander. The substrate for obtaining HES is one of the most abundant polysaccharides in nature—starch—and this is readily available from waxy maize or potato. Amylopectin is structurally similar to glycogen (a branched glucose storage polymer in humans) and this is one of the reasons why HES lacks immunogenicity. Poly-ampholyte solutions have been included as a cryo-protective agent as they are less toxic to cells, can be directly used, and create electric gradients that can be fabricated as anionic, cationic, or neutral depending on the predicted optimal matrix for regenerative intent. In directed applications of neurite outgrowth, specific materials that have capacity to hold charge have been shown that extend the outgrowth in orders of magnitude. The present invention elaborates the distinction of an acellular material in the composition with the addition of a cryoprotectant that preserves, protects, and extends potential for tailoring charge as an additive and positive affect. Exosomes have been shown to have predictive value in predicting the significance of spinal cord injury, and shown to not only cross the blood-brain barrier but protect apoptosis speck-like protein from sustaining inflammation following injury. Such use reduces catabolic influences including IL-1b that plague injury and prevent regeneration.